Asthma is an inflammatory disease of the airways. After allergen exposure, IgE bearing cells, such as mast cells and basophils, are first activated. Later, T lymphocytes enter the airways, are activated by allergen and play a key role in regulating this inflammatory response through the elaboration of cytokines such as IL-4, IL-5 and IFN-gamma. This project seeks to examine the cytokine and mediator profiles of mast cell, basophil and T cell subpopulations that may be involved in the generation of inflammation in asthmatic airways. Tryptase is a pro-inflammatory protease mediator produced principally by mast cells. We examined peripheral blood to determine if other cell populations might also be capable of tryptase expression. Tryptase expression in peripheral blood leukocytes was limited to the basophil lineage as demonstrated by these cells' expression of the basophil specific markers 2D7 and BB1 and the absence of the mast cell specific markers chymase and CD117/Kit. Surprisingly, basophil tryptase expression varied by more than 100 fold between individuals. In the high tryptase expressing individuals, per cell basophil tryptase was comparable to that of tissue mast cells. Basophil tryptase expression did not correlate with asthma, asthma severity or the presence of mastocytosis. Upon IgE cross-linking, basophils released tryptase. This study thus demonstrates that these cells are basophils rather than mast cells or a basophil-mast cell hybrid. These results suggest that tryptase represents an additional mediator through which basophils may contribute to allergic inflammation. Because basophils readily stain for tryptase, it should not be considered as an exclusive marker of mast cells. Mast cells, in addition to their well recognized expression of pro-inflammatory mediators, may also have anti-inflammatory function. To further examine this anti-inflammatory capacity of mast cells, we investigated the ability of human mast cells to produce IL-1 receptor antagonist (IL-1ra). IL-1ra mRNA and protein were constitutively expressed in resting human mast cells and upon IgE cross-linking IL-1ra mRNA was upregulated and IL-1ra protein was released. Mast cells were found to produce a 17 kd isoform of IL-1ra. This 17 kd form of IL-1ra was upregulated after allergen challenge in bronchoalveolar lavage from allergic asthmatic subjects. These findings demonstrate that human mast cells produce and release IL-1ra following IgE cross linking, which may contribute to inhibition of lung inflammation.